The bacterial phylum Chlamydiae describes Gram-negative, obligate intracellular pathogens that infect a wide range of animal hosts. One species that affects humans is Chlamydia trachomatis, a globally prevalent, sexually transmitted pathogen that infects the urogenital tract and ocular epithelia and can cause infertility, pelvic inflammatory diseases, and blindness. Another species, C. pneumoniae, targets the upper respiratory tract and can cause both pneumonia and cardiovascular disease. Chlamydia infection begins with an elementary body (EB), the invasive form of the bacteria, binding to and entering an epithelial cell. Immediately after entry, an EB transitions into a replicative reticulate body (RB) and establishes a membrane-bound parasitophorous inclusion that avoids fusion with host lysosomal compartments. At mid-to-late stages of infection, RBs revert to EB form and emerge to infect neighboring cells.
As obligate intracellular pathogens, the Chlamydiae have necessarily developed diverse strategies for evading and suppressing host defenses. For example, invading Chlamydia cells infiltrate the host cytoplasm with effector proteins targeting a range of host processes to facilitate persistent infection and bacterial propagation. One such effector protein is Chlamydial Protease-like Activity Factor (CPAF), a multimeric serine protease that is produced in the inclusion lumen and transported to the host cytoplasm.